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Ann Thorac Surg 1995;60:936-942
© 1995 The Society of Thoracic Surgeons
The Wakabayashi Institute at Irvine Medical Center, Irvine, California
Accepted for publication April 24, 1995.
| Abstract |
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Methods. Advanced age (mean age, 67 years), high oxygen dependency (70%), steroid use (46%), and markedly diminished physical capacity (2% bedridden and 27% wheelchair-bound) were noted. Thoracoscopic laser pneumoplasty was carried out under general anesthesia and one-lung ventilation. Type 3 bullae (381 procedures) were contracted by contact neodymium:yttrium-aluminum garnet laser and type 4 bullae (119 procedures) excised. The operative mortality rate was 4.8%.
Results. Subjective improvement was reported by 87% of the patients. Follow-up functional evaluation was available in 229 patients, which showed highly significant improvement. A comparison of preoperative and postoperative functional tests between type 3 and 4 bullae patients showed no significant difference, except the latter had higher decrease in airway resistance, residual volume, and total lung capacity.
Conclusions. Thoracoscopic laser pneumoplasty is an effective treatment for both type 3 and 4 bullous emphysema with an acceptable risk.
| Introduction |
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In 1991, we reported the preliminary results with thoracoscopic carbon dioxide laser treatment of diffuse bullous emphysema on the first 22 patients [1]. These patients were not considered candidates for conventional surgical excision of bullae [2, 3]. The study indicated that the procedure was effective, however, we experienced a high incidence of what appeared to be laser injury of the lung. This was demonstrated on a postoperative chest
film as infiltrates in the areas where the carbon dioxide laser was administered. This was associated with hypoxemia that persisted for several days. Multiple small perforations of the bullae by the free beam carbon dioxide laser occurred frequently and this was not readily detectable during operation and resulted in prolonged air leaks. In an attempt to correct these problems, a sapphire contact neodymium:yttrium-aluminum garnet (SLT Surgical Laser Technologies, Oaks, PA) was adopted after a laboratory investigation. To investigate the efficacy of thoracoscopic laser treatment of diffuse bullous emphysema by means of a contact neodymium:yttrium-aluminum garnet laser (referred to as thoracoscopic laser pneumoplasty, TLP), this retrospective study was conducted.
| Material and Methods |
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The medical history, pulmonary function, chest x-ray films (CXR), and computed tomographic scans (CT) of the chests were reviewed to identify bullous emphysema as the cause of symptoms and to see if there were any contraindication for operation. Malignancies of breast, colon, or prostate were in remission for more than 3 years. Three patients had peripheral non-small cell lung cancers of stage 1 or 2, and were accepted for TLP and partial lung resection [4]. If the patients had positive cardiac history, such as acute myocardial infarction or coronary artery bypass grafting, their cardiologists were contacted for clearance for general anesthesia. If the patient had a history of psychiatric disorder, the current condition was checked by contacting the primary physician. Chest x-ray films were reviewed to see obvious bullae (uncommon), hyperinflation shown as enlarged lung, increased anteroposterior diameter, local bulging of the chest wall, flattening of the diaphragm, and attenuation of the lung parenchyma. Computed tomographic scan was used to identify the presence of focal destruction of fine parenchymal structure of the lung (type 3 bullae) (Fig 1
) and measurable air cysts (type 4 bullae). The patients with spontaneous pneumothorax were not included in this series. No patient was rejected because of the severity of the illness, age, or steroid dependency. Even extremely high-risk patients, such as ventilator- dependent, were accepted; however, active smokers were rejected. All patients were using dose-metered ß-agonists and anticholinergic inhalers. In addition, many patients were taking steroid inhalers, corticosteroids, theophylline, and antibiotics. Supplemental oxygen was also commonly used. Five patients were found not receiving adequate medical treatment and were referred back to the medical management.
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From September 17, 1991, to November 11, 1993, 500 TLP procedures (372 in men and 128 in women) were performed in 443 patients. Of the 443 patients, 57 subsequently underwent TLP on the opposite side: as the second procedure of a planned two-stage operation in 45 patients; due to unsatisfactory improvement in 11; and as an emergency measure when massive expansion of the opposite lung caused acute respiratory failure in 1 patient. The age ranged from 42 to 94 years (mean ± standard deviation, 66.95 ± 6.81 years). Of 500 procedures, 381 were for type 3 bullae [4] (Fig 1
) and 119 for type 4. Three hundred fifty-one patients (70%) were oxygen dependent. The majority received steroids some time in the past and at the time of operation, 228 patients (46%) were taking prednisone at a mean dose of 11.34 ± 8.81 mg/day. The physical capacity of these patients was markedly impaired; 10 (2%) were bedridden and 134 (27%) were wheelchair-bound. Nine patients with
1-antitrypsin deficiencies were included in this series but their pulmonary function test and type of bullae were not different from other patients. In addition to routine preoperative laboratory tests, low level treadmill test using a Naughton protocol [5], room air arterial blood gases, and complete pulmonary function test, including plethysmography, were obtained to evaluate their functional status before operation.
Thoracoscopic laser pneumoplasty was carried out under general anesthesia with one-lung ventilation. The arterial line and pulse oximeter were used routinely. A Swan-Ganz catheter was placed in only a few selected cases. The indications for Swan-Ganz catheter in this series were moderately severe left ventricular dysfunction and borderline coronary artery occlusive disease in whom perioperative volume management appeared critical. The lung to be operated on was connected to continuous positive airway pressure of 1 to 5 cm H2O. Surgical procedures were carried out using a 10-mm, 30-degree rigid thoracoscope, a video camera, dual monitor screens [6] (Olympus Corp, Lake Success, NY), and standard thoracoscopic surgical instruments. The adhesions were commonly encountered and freed by a combination of blunt and sharp dissection technique. The superficial type 3 bullae were contracted by touching them with a contact neodymium:yttrium-aluminum garnet laser (SLT No. MTRL10 large round) sapphire probe that was connected either to a straight (SLT No. TXRH11) or curved (SLT No. TXRH13) thoracoscopy handpiece, at 8 to 12 W. The contact laser probe was moved over the bullae as if one was ironing a shirt. Normal saline was squirted over the bullae at intervals to keep the surface wet. If the interlobar fissure was fused by adhesion, it was divided to expose hidden bullae. In general, bullae were found at the sites of adhesions. Therefore, all adhesions were freed. After the superficial bullae were contacted by the laser, the lung was manually inflated. If no bullae bulged out and the consistency of the underlying lung was near normal, the laser contact was considered adequate. If a few bullae bulged out, they were contacted again. Type 4 bullae were opened widely and trabeculae were detached from the bullous wall, using a contact laser scalpel (SLT No. GRP6 or GRP10) at 15 W until the base of the bullae was reached. Then the bullae were excised. Before an endoscopic stapler became available in 1993, the bullae were excised and sutured manually. After an endoscopic stapler became available, it was used whenever applicable to shorten the operating time.
After operation, the patients were supported by a ventilator until they met standard weaning criteria. If air leaks persisted without pneumothorax on CXR, they were treated conservatively by continuous suction on the chest tubes. If air leak was massive, causing difficulty in managing ventilation (4 patients) or did not slow down after more than 2 weeks (32 patients), the patients were returned to the operating room and the bronchopleural fistulae were closed by suturing or stapling by means of thoracoscopy.
All deaths that occurred within 30 days after operation or during hospitalization were defined as the operative mortality. If a patient was transferred to another extended care facility and died, this was also included in the operative mortality. All deaths that occurred within 3 months after discharge were called early mortality. A combination of operative and early mortality rates was referred to as a 3-month mortality rate (MR3).
The patients were discharged from the hospital when air leaks stopped and other medical conditions were stable. After discharge, the patients took a 2-week course of pulmonary rehabilitation as outpatients. When they were released home, they were requested to send us the follow-up functional studies and CXR at 3 and 6 months. Follow-up study was conducted by contacting the patients by mail or telephone who failed to send the 3- to 6-month follow-up functional studies. Those who underwent the second side operation repeated the complete preoperative tests, which were included in the follow-up data.
Oxygen and steroid dependency, severe hypoxemia (oxygen tension less than 44 mm Hg), and carbon dioxide retention (carbon dioxide tension more than 60 mm Hg), and forced expiratory volume for 1 second (FEV1) less than 14% of the predicted value were analyzed to determine whether these risk factors affected operative, early, and 3-month mortality rates, as well as incidence of tracheostomy. These data were analyzed using the
2 tests. The test data were sent to an independent research consultant firm (RSS Research Support Service, Irvine, CA) for statistical analysis. The analyses addressed the following questions: (1) Was there any difference between patients' function before and after operation? (a series of paired t test) (2) Were there any differences between type 3 and type 4 bullae patients with regard to the pulmonary function before and after operation? (a series of group t test).
| Results |
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The operating room time ranged from 1.20 to 10.60 hours (mean, 3.89 ± 1.40 hours). All patients tolerated one-lung ventilation. Thoracoscopy was converted to open thoracotomy in 1 patient when bleeding from the intercostal vein could not be controlled. The duration of postoperative ventilatory support varied from 0 to 714.30 hours (mean, 22.04 ± 60.17 hours). Ventilatory support was for less than 44 hours in 95% of the patients and their postoperative ventilatory support was 12.39 ± 7.89 hours. Of 25 patients who were on a ventilator for more than 45 hours, 8 died and 3 required tracheostomy. These 3 patients were transferred to other facilities, where they were weaned off the ventilator. The length of hospital stay varied from 2 to 97 days (mean, 18.26 ± 14.14 days). Twenty-three patients were discharged with a chest tube connected to a Heimlich valve and when the air leaks stopped, the chest tubes were removed, from 5 to 12 days. The wound infection occurred in 1 patient at the chest tube site, which resolved after removal of the tube.
There was no intraoperative death. Twenty patients died during hospitalization. Four additional patients died at the extended care facilities. The overall operative mortality rate was 4.8%. The causes of deaths were acute respiratory failure in 15 patients; tension pneumothorax in 3; acute myocardial infarction in 2; pulmonary embolism in 1, pneumonia in 1; aspiration pneumonitis in 1; misplacement of tracheostomy tube in 1; and overdose of sedatives in 1 patient. Seven patients died within 3 months after discharge from the hospital. The causes were tension pneumothorax in 3 patients and acute respiratory failure in 4.
Numerous nonfatal complications occurred during hospitalization. The most common complication was persistent air leaks as reported earlier [1]. Subcutaneous emphysema was common, ranging from subclinical to massive subcutaneous air, requiring subcutaneous placement of a chest tube (8 patients). Four patients required transurethral prostatectomy, 3 received transvenous pacemaker for sick sinus syndrome, 3 had development of ileus and were treated conservatively, 1 had massive hematemesis, requiring emergency vagotomy and pyloroplasty, 1 had perforated sigmoid diverticulitis and was treated by diverting colostomy, and 1 patient had acute thrombosis of the femoropopliteal artery and underwent a revascularization procedure.
During the follow-up period of 12 to 39 months, 23 patients died. The causes of late deaths were acute myocardial infarction in 8 patients, acute respiratory failure and pneumonia in 8; stroke in 1; brain metastasis of small cell carcinoma in 1; mesenteric artery thrombosis in 1; tension pneumothorax of the opposite lung in 1; old age in 1; pulmonary emboli in 1; and hemorrhagic shock in 1 patient. Twenty-two patients developed delayed spontaneous pneumothorax after going home, ranging from 1 to 7 months. Five of them returned to us and underwent thoracoscopic closure of bronchopleural fistulae. Two patients underwent conventional thoracotomy at their local hospitals.
Four hundred twelve patients were eligible for follow-up studies. Follow-up pulmonary function tests, at least in part, were available in 229 patients. However, 26 of them could not tolerate preoperative assessment and were excluded from the analysis. Two hundred twenty-two patients responded to the questionnaires without functional tests. One hundred ninety-one (87.4%) reported that breathing and physical capacities were better than before operation, 13 unchanged (7.7%), and 7 worse (3.6%). Eleven did not answer. The causes of poor results were increased bullae of the opposite side in 3 patients, residual or recurrent bullae in 1; pulmonary embolism in 1; and pneumonia in 1 patient. One patient had development of delayed pneumothorax and underwent thoracotomy after which she had a very slow recovery. One patient had development of tension pneumothorax of the opposite side and underwent thoracotomy at other institution and died. The causes of no improvement were the expansion of the bullae of the other side in 6 patients; recurrent bullae in 2; and unknown in 4 patients.
The risk factor analysis revealed that totally oxygen-dependent patients had a significantly higher MR3 (9.9%) than those who were using oxygen at times (2.5%) or not at all (3.3%) (p < 0.01) (Table 1
). Ambulatory patients had a significantly lower MR3 (3.1%) than bedridden (50%) or wheelchair-bound patients (11.9%) (p < 0.01) (Table 1
). Steroid-dependent patients had a significantly higher MR3 (9.8%) than those who were not (4.6%) (p < 0.05) (Table 1
). The patients with arterial oxygen tension less than 44 mm Hg had significantly higher MR3 (11.8%) than the others (p < 0.01) (Table 1
). The patients with carbon dioxide tension more than 60 mm Hg had a significantly higher MR3 (21.1%) than the others (p < 0.01) (Table 1
). The patients with FEV1 less than 14% of the predicted value had a significantly higher MR3 (11.1%) than the others (p < 0.01) (Table 1
). The incidence of tracheostomy was not affected by oxygen dependency or low FEV1. Bedridden patients, those with oxygen tension less than 44 mm Hg, and those with carbon dioxide tension higher than 60 mm Hg had significantly higher incidence of tracheostomy than the others (p < 0.01) (Table 1
). None of the risk factors analyzed had any value in predicting the postoperative FEV1 (Table 2
). Among risk factors tested, only FEV1 had a significant value in predicting the subjective improvement; 87% of the patients with FEV1 more than 15% reported improvement, whereas only 53% of those with FEV1 less than 14% did (p < 0.01) (Table 3
). The paired comparison t tests between the preoperative and postoperative (follow-up) functional tests are shown in Table 4
. The differences in oxygen tension, carbon dioxide tension, and FEV1/forced vital capacity were insignificant. All other parameters, treadmill test, forced vital capacity, FEV1, airway resistance, residual volume, and total lung capacity showed significant improvement. The comparison of type 3 bullae and type 4 bullae patients is shown in Table 5
(preoperative) and Table 6
(postoperative). There was no significant difference in arterial blood gas, treadmill test, and pulmonary function test before operation. Postoperatively, the type 4 bullae patients showed significantly better improvement of airway resistance, residual volume, and total lung capacity. There was no significant difference between them in other parameters.
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| Comment |
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The fatal occult tension pneumothorax occurred in an early stage of this study. This problem was solved by the liberal use of limited CT scans of the chest. When the patient developed progressive shortness of breath after uneventful postoperative recovery, and arterial blood gases, CXR, and physical examination were unremarkable, limited CT scans without contrast were obtained immediately. If occult pneumothorax was found, a chest tube or percutaneous drainage catheter was placed under CT guidance. In addition, a significant incidence of delayed spontaneous pneumothorax was noted. This occurred not only on the side of the operation but also on the opposite side (2 patients). Although the incidence of pneumothorax became less frequent as the time passed after TLP, the patients with bullous emphysema should be considered at risk of spontaneous pneumothorax at any time. I treated 1 patient for spontaneous pneumothorax who had surgical bullectomy 8 years ago (not included in this series). As predicted, pneumonia and acute respiratory failure were the most common cause of operative and early deaths. In contrast, the causes of late deaths were more diverse and acute myocardial infarction was the most common cause of late deaths. I would propose MR3 in reporting the result of any type of surgical intervention of bullous emphysema, as the 3-month mortality rate appears to reflect the actual risk associated with the procedure more accurately than the conventional 30-day mortality rate.
It is very encouraging that the majority of our patients stated that their breathing was much improved and they could do many things that they could not do for many years. The mean preoperative treadmill test, 5 minutes on the Naughton protocol [5], is less than the first stage of the more vigorous and popular Bruce protocol for cardiac treadmill test [8], which is less than 2.6 metabolic units. Less than 12 minutes (6 metabolic units) are considered very low exercise tolerance. The follow-up functional tests could be biased because many patients who were doing well refused to have follow-up functional tests because of expenses. They consulted their physicians only when they started to feel shortness of breath again. Therefore, the follow-up data might have been better if taken when they felt better. Also some patients were too sick to take preoperative tests but could do so only after operation. Due to the lack of the baseline data, their follow-up results could not be used. Despite these limitations, the follow-up data showed highly significant improvement.
As predicted, there was a good correlation between risk factors and MR3 and the risk factors and incidence of tracheostomy. However, they failed to predict the objective or subjective result except low FEV1 was associated with a less satisfactory result. Although type 4 bullae are readily recognizable on CT, the majority of them did not satisfy the classic indication for surgical excision of bullae [2, 3] (eg, crowding of vessels and compression of the functioning lung). Recently Cooper and colleagues [9] reported the preliminary result on 20 patients who underwent transsternal stapling of bilateral bullae (pneumectomy). They removed what appeared to be type 3 bullae with no operative deaths and reported significant functional improvement for a period of 1 to 15 months' follow-up (mean, 6.4 months). Their results must be interpreted with caution. The number of their patients is small. In my series, there were no deaths in the first 31 patients. Also, their follow-up period was very short. I do not order a pulmonary function test before 3 months after operation because strenuous breathing needed for the pulmonary function test is traumatic to the recovering lungs. I recently operated on a patient whose bullae recurred 1 year after transsternal bilateral bullectomy using staplers done in 1986. It is of interest how many of Cooper and associates' patients will have recurrence over the next few years. Their concept that the volume reduction of hyperinflated lung will improve the lung function needs further testing. Figure 2
shows a postoperative CT of type 3 bullae (shown in Fig 1
), 20 months after TLP. I believe that the restoration of fine parenchymal structure of the lung as shown in this figure and not the volume reduction is a key to improve the lung function. The reduction of lung volume should be the result and not the objective of any surgical intervention on bullous emphysema. The type 4 bullae patients showed significantly greater reduction in airway resistance, residual volume, and total lung capacity than the type 3 bullae patients. This may be due to mechanical removal of bullae. However, all other parameters were not different. A further investigation is necessary to elucidate the mechanism of functional improvement after TLP.
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